Self injurious behavior in captive nonhuman primates can be a serious problem occurring in about 10% of individually housed monkeys at some point during their adult life. Previous assessment of the hypothalamic-pituitary-adrenal axis in 24 individually housed monkeys (13 with SIB and 8 age-matched controls) revealed a dysregulation of the HPA axis in monkeys with a veterinary record of self-inflicted wounding. Monkeys with SIB showed significantly lower AM basal plasma cortisol compared to controls (SIB = 23.6 + 3.2 ug/dL; CONT = 43.4 +6.4 ug/dL; p<.05). The purpose of this study was to extend our understanding of the possible underlying mechanisms of HPA dysregulation by sampling both in the AM and PM and to investigate the role of the hypothalamic-pituitary gonadal axis (HPG) in these populations. Blood samples were collected from each individual in the early morning (8:30 AM) and in the late afternoon (4:30 PM) on separate days. The samples were assayed for ACTH and cortisol (as indicators of HPA activity) and for testosterone (an indicator of HPG activity). Data were analyzed by ANOVA with group (SIB vs. CONT) as a between subject variable and time of day as the within subjects variable. As reported previously, monkeys with SIB exhibited significantly lower cortisol levels as compared to controls. As expected, cortisol levels were significantly lower overall in the PM sample. There was no interaction between group and time although inspection of the data showed a tendency for the groups to differ more in the morning than the late afternoon. Monkeys with SIB did not differ from controls in basal plasma ACTH or testosterone. As with cortisol, ACTH levels were significantly lower in the PM samples whereas testosterone was elevated in the PM samples. These results lend further support to the presence of a subtle dysregulation of the HPA axis in monkeys with SIB. Given the direction of the effect (i.e., lower cortisol), we are now examining possible linkages to post-traumatic stress disorder which also has low cortisol as a marker. Challenge procedures (e.g., reverse dexamethasone suppression) will be employed in the near future to determine the locus at which the dysregulation occurs.